Objective To observe the effect of electroacupuncture(EA) intervention on behavior changes

expression of cerebral vascular endothelial growth factor(VEGF)

nerve growth associated protein-43(GAP-43)

synaptophysin(SYN)

myelin basic protein(MBP)

neurite outgrowth inhibitor-A(Nogo-A) in cerebral focal ischemia-reperfusion injury(CI/RI) rats

so as to study its mechanism underlying improvement of ischemic cerebral vascular disease.Methods Sixty male SD rats were randomly divided into sham-operation group

model group and electroacupuncture(EA) group.CI/RI model was established by occlusion of the middle cerebral artery(MCAO) and reperfusion.EA was applied to bilateral "Neiguan"(PC 6)

"Sanyinjiao"(SP 6)

"Shuigou"(GV 26) and "Baihui"(GV 20) for 30 min

once a day for 14 days.The neurologic deficits were evaluated by Longa 5-grade standard(the higher the score

the severer the neurologic deficit).The immunoactivity of cerebral VEGF

GAP-43

SYN

MBP(important in the process of myelination of nerves in the nervous system) and Nogo-A(inhibiting axonal regeneration) in the focal ischemic cerebral tissue was detected by immunohistochemistry.Results The Longa's score of the model group was significantly increased after MCAO in comparison with the sham-operation group(P<0.01).In comparison with the model group

Longa's score of the EA group was evidently lower on day 14 after CI/RI(P<0.05)

suggesting an improvement of the neurological deficits after EA intervention.In comparison with the sham-operation group

the immunoactivity of cerebral VEGF

GAP-43 and Nogo-A was significantly upregulated on day 7 and 14 in the model group(P<0.01)

while that of cerebral SYN was remarkably down-regulated in the model group on day 7 and 14 after CI/RI(P<0.05).Compared with the model group

cerebral VEGF

GAP-43

SYN and MBP expression levels were considerably upregulated on day 7 and 14 following CI/RI in the EA group(P<0.01

P<0.05)

while that of cerebral Nogo-A was significantly decreased at the two time-points in the EA group(P<0.01).Conclusion EA intervention can effectively improve neurological function in cerebral infarction rats

which is closely related to its effects in upregulating cerebral VEGF

GAP-43

SYN and MBP expression

and down-regulating Nogo-A protein

suggesting a protective effect on neurovascular unit.